Cardiovascular Disease and Lifestyle Modification




Because of the difficulty many patients have in improving their diet, physicians may be tempted to lose faith in a nonpharmacologic approach to the treatment of cardiovascular disease (CVD). This chapter describes the strong scientific base that supports healthy nutrition and regular exercise and provides practical approaches to illustrate how patients can achieve positive lifestyle modification.


Epidemiologic observations worldwide show a pattern of CVD prevalence that points directly at poor nutrition, too much food, and erosion of a healthy lifestyle as the causes of high rates of CVD worldwide. Very low rates of CVD still exist in parts of Mediterranean countries and Japan and China, where traditional diets and lifestyles are maintained. During the transition to a developed economy typical of North America and Europe, the incidence of CVD and diabetes increases rapidly, as has been evident worldwide and most notably in South Asia and Latin America.


Although drug therapy for hyperlipidemia has had huge success in decreasing CVD, national guidelines rightfully still call for nutrition and exercise for primary prevention. For secondary prevention, nutrition and drug therapy should be used together. Diet and drug treatments are additive in improving risk factors such as low-density lipoprotein cholesterol (LDL-c), blood pressure, and insulin resistance and in reducing CVD. Improved diet quality reduces CVD, even when body weight remains excessive. However, weight loss has its own benefits: it can raise high-density lipoprotein cholesterol (HDL-c), lower triglyceride (TG) levels, improve insulin sensitivity, and lower blood pressure. When adopted intensively and taken to their full potential, diet and weight loss may eliminate the need for drug therapy for hyperlipidemia, hypertension, or type 2 diabetes, and it may simplify the ever more complex multidrug regimens necessary to control these conditions.


Dietary Fats and Blood Lipids


Saturated fats, trans (unsaturated) fats from partially hydrogenated vegetable oils, and cholesterol increase blood LDL-c levels. Saturated fat and cholesterol are present mainly in dairy fat and red meat, whereas trans fats are present in most fried foods and baked products in the United States. Trans fatty acids are also present in dairy and meat fat, formed in the ruminant gut by bacteria during digestion. All guidelines call for reduction in these dietary lipids. When saturated fats, trans fats, and cholesterol are reduced in the diet, LDL-c decreases in proportion to the magnitude of the dietary changes. This happens with whatever nutrients replace them, which is the rationale for traditional guidelines that recommend a low-fat, carbohydrate-rich diet as a pragmatic way to reduce unhealthy fats. The remaining question is whether nutrients and foods other than those rich in carbohydrates could replace the unhealthy fats; other possible replacements are unsaturated fats and oils and protein. Beneficial potentials of unsaturated fats have been established, and new mechanisms are still being discovered. Moreover, dietary protein improves CVD risk factors. The effects on blood lipids and blood pressure of approaches that emphasize either carbohydrate, unsaturated fat, or protein were compared in the Optimal Macronutrient Intake (OMNI) Heart trial, which is discussed later in this chapter.


High-Carbohydrate, Low-Fat Diets to Reduce Low-Density Lipoprotein Cholesterol and Blood Pressure


Low-fat, high-carbohydrate diets reduce LDL-c generally by a modest amount, 5% to 10%, in proportion to adherence. Very-low-fat, low-cholesterol diets can reduce LDL-c more, but acceptability by the general public may be limited; in addition, very-low-fat diets may be deficient in essential fatty acids. Low-fat, high-carbohydrate diets reduce LDL-c as well as reduce HDL-c and raise TGs ( Figure 26-1 ). Because the LDL/HDL ratio is unchanged, CVD risk cannot be assumed to decrease on a low-fat diet. In fact, replacing saturated and trans fats with monounsaturated and polyunsaturated fats, rather than carbohydrate, is more strongly associated with improved lipid risk factors and reduced CVD in epidemiologic studies and clinical trials. Furthermore, the type of carbohydrate-containing foods that replace saturated fat–rich foods influences risk factors and coronary heart disease (CHD). In addition, some carbohydrate-rich foods raise blood glucose less than others, and it is these that possess the favorable effects.




FIGURE 26-1


Effect of cholesterol-lowering diets on blood lipid risk factors. HDL, high-density lipoprotein; LDL, low-density lipoprotein.

(Modified from Sacks FM, Katan M. Randomized clinical trials on the effects of dietary fat and carbohydrate on plasma lipoproteins and cardiovascular disease. Am J Med 2002;113[Suppl 9B]:13S-24S.)


The DASH Diet


The Dietary Approaches to Stop Hypertension (DASH) study attempted to combine information from epidemiology and animal studies on possible new dietary means to prevent and treat hypertension. Although weight loss and dietary sodium reduction had long been shown to lower blood pressure, population studies suggested that other nutrients may also have beneficial effects. The DASH research group designed a dietary pattern rich in fruits and vegetables and low-fat dairy products that included nuts and whole grains and was low in red meat and sugar-containing desserts and beverages. The DASH diet substantially reduced blood pressure and extended the potential for nutritional control of hypertension. When the DASH diet was combined with reduced sodium, the beneficial effects were even stronger ( Figure 26-2 ). In the typical older patient population in clinical practice, the DASH diet with low sodium content reduced systolic blood pressure by 15 mm Hg in those with mild hypertension and 10 mm Hg in those with above-average blood pressure (120 to 139 mm Hg), now termed prehypertension. Older patients responded to the DASH diet and low sodium more than younger patients, which flattened the relation between blood pressure and age to such an extent that little change in blood pressure with age would be expected in those who optimize their diet.




FIGURE 26-2


Effect of the low-sodium Dietary Approaches to Stop Hypertension ( DASH ) diet on systolic blood pressure in older patients with mild hypertension. BP, blood pressure.

(Data from Sacks FM, Bray GA, Carey VJ, et al. Comparison of weight-loss diets with different compositions of fat, protein, and carbohydrates. N Engl J Med 2009;360:859-873.)


The DASH diet also reduced LDL-c, as would be predicted from its low content of saturated fat and cholesterol. However, HDL-c also decreased predictably by approximately the same percentage as LDL-c, and the ratio did not change. Interestingly, TGs did not increase on the DASH diet, as they often do on a high-carbohydrate diet. Perhaps this is because of the relatively good type of carbohydrates consumed, those with a low glycemic index, which cause reduced blood glucose response. Overall, predicted CVD risk was reduced on the DASH diet because of its benefits of lower blood pressure and LDL-c outweighing the reduced HDL-c. With low sodium, CVD risk on the DASH diet improved more. DASH is considered the benchmark dietary pattern recommended by the U.S. Dietary Goals Committee. More and more, dietary patterns and the component foods, rather than specific nutrients, are being used as the basis of dietary recommendations as reviewed recently.


Low-Fat Diets, Low Saturated Fat, and Cardiovascular Disease: Clinical Trials and Epidemiology


Low-fat diets never had a satisfactory test in a randomized clinical trial with clinical endpoints. The Women’s Health Initiative (WHI) was an attempt to test this diet in a trial of 160,000 women in the United States. These women were randomized to either a low-fat, high-carbohydrate diet recommended to be rich in fruits and vegetables or to a no-intervention comparison group and were followed for 7.5 years. No effect on CVD endpoints or cancer occurred. Although the WHI set a goal for reducing total fat to 20%, it was clear from lack of HDL reduction or TG increase, both biomarkers of dietary fat reduction, that the participants were able to reduce fat only minimally. Previous small-scale trials did not find reduction in CVD with low-fat diets. In a small group of patients with CHD, Ornish and colleagues used a very low-fat vegetarian diet as a major part of an overall lifestyle change that included intensive exercise, and meals were provided to the patients. Coronary stenosis improved in the treated group, although the study was not large enough to evaluate an effect on clinical events. A less intensive program of low-fat diet and exercise in Heidelberg, Germany, also found benefits on coronary stenosis. Epidemiologic data generally have not found a relation between amount of total fat and CHD. Even more, the amount of dietary saturated fat, which has proven effects on LDL-c and atherogenesis, does not predict CHD in many epidemiologic studies. This has provided grist for recent controversy on saturated fat and CHD and the advisability of low-fat diets. In fact, implicit in the traditional, multiple-variable statistical models that evaluate saturated fat are the replacement foods and nutrients in the specific populations studied. If most people who eat a small amount of saturated and total fat instead eat high-carbohydrate junk food, saturated fat gains the illusion of neutrality. A newer epidemiologic approach developed by Willett and colleagues tests specific exchanges of foods and nutrients in the population. This technique effectively resolved the controversy by showing that low saturated fat intake is predictive of low CHD rates only if healthful low–glycemic index carbohydrates or polyunsaturated fats are increased. A low-fat dietary pattern can be based on healthy foods—such as whole grains, fruits and vegetables, low-fat dairy products, and fish and lean meats—or it can have plenty of high-carbohydrate, high-calorie foods such as refined flour products, desserts, and sugar-containing drinks. The type of low-fat diet may be important to its success or failure for risk factor improvement.


Effects of standard low-fat, high-carbohydrate diets on CVD risk factors and CHD are as follows:




  • Reduction of LDL-c concentration



  • Reduction of HDL-c concentration



  • No effect on the LDL/HDL cholesterol ratio



  • Increase in TG levels (usually)



  • Improvement in coronary stenosis (with an intensive exercise program)



  • No reduction in CHD in epidemiologic studies or small-scale, short-duration trials



  • No reduction in CVD in the definitive WHI



A low-fat diet that truly expresses a healthful dietary pattern has not been tested in a large, randomized trial with clinical CHD outcomes, although epidemiologic studies suggest that it would be beneficial.


Moderate Unsaturated Fat Diets


Replacing saturated fat with unsaturated fat has a long history of CVD prevention. In the 1950s and 1960s, an era lacking effective and well-tolerated CVD prevention drugs, polyunsaturated vegetable oils from corn, soybeans, and safflower seeds were used essentially as medicine to lower blood cholesterol. These polyunsaturated oils are the most potent LDL-lowering nutrients, and several clinical trials have demonstrated significant reductions in CVD from their use. A unique type of unsaturated oil is rapeseed oil (Canola), which is mainly monounsaturated fat but also has omega-3 fatty acid and α-linolenic acid (ALA) components. The Lyon Heart Study used rapeseed oil with a Mediterranean diet in a secondary prevention study and found a reduction in CVD. ALA, also prevalent in soybean oil and some vegetable products, is strongly protective against CHD in epidemiologic studies. However, a recent trial showed supplements of ALA given to elderly patients after myocardial infarction (MI) did not reduce CHD compared with a placebo. An explanation suggested by Campos and colleagues is that ALA reduces CHD only when it is increased from a very low dietary level, as exists in many countries, which can be studied by epidemiology. Finally, olive oil and high-monounsaturated varieties of sunflower and safflower oils have primarily monounsaturated oils. This class of vegetable oil improves risk factors, although they have not been tested in a clinical endpoint trial.


Whatever unsaturated fat is used to replace saturated and trans fats, whether unhydrogenated liquid vegetable oils—such as rapeseed, olive, sunflower, safflower, peanut, or soybean oil—or from nuts, total fat intake can be made to remain the same, or it can be increased to replace some carbohydrate. It is uncertain whether polyunsaturated or monounsaturated fat is superior for preventing CHD, although current evidence favors polyunsaturated oils. Polyunsaturated fats have slightly more effect than monounsaturated fat in lowering LDL levels and perhaps in reducing serum inflammatory markers. Any type of fat raises HDL-c and lowers TGs compared with carbohydrate. However, the type of carbohydrate food may relate to its metabolic effects. Diets high in unsaturated fats improve the lipid profile compared with saturated fat as well as carbohydrate.


Randomized trials definitively show the benefits of polyunsaturated fats. Three of four randomized trials showed significant benefits on coronary disease rates ( Table 26-1 ). In addition to lowering LDL, polyunsaturated fats may reduce the vascular inflammatory response and may limit the propensity of LDL particles to bind to vascular cells and deposit their cholesterol in vascular intima. In monkeys, polyunsaturated fats from vegetable oils actually reduced coronary atherosclerosis. Polyunsaturated fats from vegetable oils also have antiarrhythmogenic actions, although this property has not been tested in a clinical trial. Thus, much evidence exists for the use of polyunsaturated oils to replace saturated fats to prevent coronary disease.



TABLE 26-1

Clinical Trials of Diet Therapy with Polyunsaturated Vegetable Oils to Reduce Coronary Events: Substitution of Polyunsaturated Fat for Saturated Fat







































STUDY N DIETARY FAT DURATION (YEARS) Δ CHOLESTEROL * Δ CVD
Finnish Mental Hospital 676 34% 6 −15% −43%
Oslo 412 39% 5 −14% −25%
Medical Research Council soy oil 393 46% 4 −15% −12%
Los Angeles 846 40% 8 −13% −34%

Cardiovascular disease (CVD) is defined as myocardial infarction or sudden death for the Finnish, Oslo, and MRC trials and myocardial infarction, sudden death, or stroke for the Los Angeles trial. Trials with at least 2 years of average follow-up were included.

* Percentage change in serum cholesterol in the treatment group compared with the change in the control group.


Percentage difference in coronary event rates in the treatment compared with the control group.


P ≤ .05.



Monounsaturated fat has a weaker direct relationship to coronary disease prevention compared with polyunsaturated fat. A clinical trial that specifically raised monounsaturated fats to prevent CHD has not been performed. Monkey models of atherosclerosis do not show a benefit of monounsaturated fats; however, in humans, monounsaturated fats are nearly as effective as polyunsaturated fats to decrease LDL and preserve HDL and TG levels. Monounsaturated oils, particularly olive oil, have been an integral part of the centuries-old traditional Mediterranean diet, which has been associated with very low CVD rates. Thus, there are reasons to advocate increased intake of unsaturated oils from a variety of sources, both monounsaturated and polyunsaturated.


Reduced-Carbohydrate, Higher Unsaturated Fat, and Protein Diets: A New Twist to the DASH Dietary Approach


The DASH diet, considered the benchmark diet for health in the United States, is low in fat and high in carbohydrate. Although it reduced blood pressure and LDL-c, it reduced HDL-c also and did not affect TG levels. In view of the favorable evidence on the effects of unsaturated fats on HDL and TGs, it was hypothesized that the DASH diet could be improved in its overall effects on CVD risk factors by replacing some of the carbohydrate with unsaturated fats. In addition, higher protein intake, replacing carbohydrate, was predictive of reductions in blood pressure and CVD in epidemiologic studies, and small-scale studies found favorable effects on lipid risk factors. The OMNI Heart study designed three healthful diets: one high in carbohydrate, similar to the DASH diet; another high in unsaturated fat; and a third high in protein from mixed sources. All three were low in saturated fat and cholesterol and high in fruits, vegetables, nuts, and low-fat dairy products, thereby building on the dietary approach of DASH. All three diets substantially improved blood pressure and LDL-c; however, lowering carbohydrate intake by raising either unsaturated fat or protein further reduced blood pressure and TG levels. The unsaturated-fat diet raised HDL-c, whereas the protein diet lowered LDL-c and HDL-c ( Table 26-2 ). Taken together, moderate reduction in carbohydrate intake, from 58% to 48% of total calories, produced 11% to 13% further reduction in estimated CVD risk beyond the 20% effect of the DASH-type diet. Several publications described in detail this dietary approach to advise physicians, dietitians, and patients.



TABLE 26-2

Beneficial Effects on Blood Pressure and Blood Lipids of Replacing Carbohydrate with Protein or Unsaturated Fat (OMNI Heart Study)











































Mean Change from Baseline
FACTOR BASELINE CARBOHYDRATES PROTEIN UNSATURATED FAT
LDL (mg/dL) 157 −20 −24 −22
HDL (mg/dL) 50 −1 −3 0
Triglyceride (mg/dL) 102 0 −16 −9
Systolic BP (mm Hg) 146 −13 −16 −16
Risk reduction 16% 21% 20%

BP, blood pressure; HDL, high-density lipoprotein; LDL, low-density lipoprotein; OMNI, Optimum Macronutrient Intake trial.


Effects of reduced-carbohydrate, high–unsaturated-fat diets on CVD are as follows:




  • Reduction in blood pressure



  • Reduction in LDL-c concentration



  • Preservation of HDL-c concentration



  • Reduction in the LDL-c/HDL-c ratio



  • Decrease in TG levels compared with low-fat diets



  • Reduction in CVD events (polyunsaturated fats)



The effects of increased protein and lower carbohydrate intakes are as follows (CVD was not directly studied in a randomized trial):




  • Lowered blood pressure



  • Lowered LDL-c



  • Lowered HDL-c



  • Lowered TGs



  • Lowered CVD risk (in epidemiologic studies)



Type of Carbohydrate


The usual mix of carbohydrates in the Western diet contains large amounts of refined polysaccharides, such as in bread and baked goods, and sugars in juices and soda. These have a high glycemic index, causing glucose and insulin to rise substantially. Other types of carbohydrates, those found in whole grains and vegetables, have a lower glycemic index because the digestion and absorption of the glucose occur more slowly and cause less of a rise in blood glucose and hence a lower rise in insulin. The low glycemic index of grains and vegetables is partly explained by the fiber content of these foods but also by the intrinsic digestibility of the food. These foods also cause less of a rise in plasma TG levels than the more commonly eaten carbohydrates that are higher on the glycemic index. Some of the concerns about a low-fat diet can be set aside if a patient truly eats foods with a low glycemic index, rather than the ubiquitous, less desirable high-carbohydrate foods that all too often are a major part of low-fat diets. As mentioned, a diet of low–glycemic index, carbohydrate-rich foods was predictive of reduced CHD when these replaced saturated fat in a meta-analysis, whereas diets with carbohydrates high on the glycemic index were not.


Fish Oil to Prevent Coronary Heart Disease


In the early 1980s, two lines of evidence coalesced to engender widespread excitement on the potentially cardioprotective effects of omega-3 fatty acids from fish oil (EPA, DHA). Populations that eat large amounts of fatty fish had low rates of CVD, and in many epidemiologic studies, n-3 polyunsaturated fatty acid (PUFA) intake and blood levels are inversely related to CVD, a finding confirmed by randomized trials. For example, The Diet and Reinfarction Trial (DART) tested the effect of increased intake of fatty fish or fish oil (1.5 g/day) for 2 years in 2033 Welsh men who had had an acute MI. This small amount of fatty fish or fish oil significantly reduced coronary and total mortality rates; however, nonfatal MI was not significantly affected. These results have been reinforced by the Groupo Italiano per lo Studio della Sopravvivenza nell’Infarto Myocardico (GISSI) Prevenzione trial, which tested 1 g/day of n-3 PUFAs in 11,324 Italian patients surviving a recent MI. In both trials the death rate began to lessen in the fish oil group as early as 3 months after treatment was started, and a Japanese trial of primary prevention of CVD with fish oil showed striking reductions in nonfatal CVD events. Thus, relatively low doses of fish oil, 1 to 2 g/day, may be cardioprotective because of several mechanisms yet to be specifically determined.


Omega-3 fatty acids are metabolized to prostaglandins, leukotrienes, and resolvins that are antithrombotic, antiinflammatory, and vasodilating. However, the most established clinical benefit of fish oil is the reduction of blood TG levels. A large dose is necessary, and 10 to 15 capsules (1 g) of fish oil that contain between 20% and 50% omega-3 fatty acids are required. A prescription version of fish oil that is 90% omega-3 fatty acids is available, which requires fewer capsules. Use of fish oil for hypertriglyceridemia is discussed in Chapter 25 .


Fish oil and other PUFAs have potential antiarrhythmic effects, increasing the depolarization threshold of ion channels. Reduction in fatal CHD events has been reported in epidemiologic studies, often attributed to reduced sudden death. However, a broader view of the benefits of omega-3 fatty acids is necessary because sudden death cannot account for all CVD event reductions, nonfatal as well as fatal, found in epidemiologic studies and clinical trials. Clinical trials that tested fish oil in patients with cardiac arrhythmias did not confirm protection against ventricular tachyarrhythmias in those with implanted defibrillators or against atrial fibrillation.


Effects of fish oil intake are as follows:




  • Large doses (>5 g/day omega-3 fatty acids)




    • Reduction in blood TGs



    • Reduction in blood pressure



    • Prevention of thrombosis




  • Small doses (1 to 2 g/day omega-3 fatty acids)




    • Prevention of CVD events, fatal and nonfatal






Obesity


The obesity epidemic continues to plague the United States. More than one third of U.S. adults—more than 72 million people—and 17% of U.S. children are obese. From 1980 through 2008, obesity rates for adults have doubled, and rates for children have tripled. The sex-specific prevalence of obesity was 32% of men and 36% of women from 2007 through 2008, and 25% of men and 31% of women aged 20 to 34 years were obese compared with 40% and 42% of 55- to 64-year-olds. After age 64 years, the prevalence of obesity declines; the rate is 26% in men and women 75 years and older. The prevalence of obesity is greater among non-Hispanic blacks and Mexican Americans than among non-Hispanic whites. The health consequences of obesity are significant and include a higher risk of CHD, type 2 diabetes, high blood pressure, high total cholesterol and TG levels, sleep apnea, liver and gallbladder disease, and reproductive health complications. Obesity was estimated to cost $79 billion in 1998 in the Unites States. By 2008, the cost was estimated to have risen to $147 billion.


The debate regarding what diet is most effective for treating obesity and overweight has been informed in the past 3 years by large, long-term randomized trials. In the past few years, a number of longer term trials (≥2 years) have published data examining not just weight loss but sustainability of lost weight. Sacks and colleagues conducted a randomized trial in 811 overweight or obese people and concluded that reduced calorie diets result in clinically meaningful weight loss regardless of which macronutrients they emphasize. After 2 years, weight loss remained similar in those who were assigned to a diet with 15% protein and those assigned to a diet with 25% protein (3.0 and 3.6 kg, respectively); in those assigned to a diet with 20% fat and those assigned to a diet with 40% fat (3.3 kg for both groups); and in those assigned to a diet with 65% carbohydrate and those assigned to a diet with 35% carbohydrate (2.9 and 3.4 kg, respectively) ( P > .20 for all comparisons; Figure 26-3 ). Participation in group counseling sessions was strongly predictive of weight loss at 2 years, and conclusions were that weight-loss diets can be tailored to individual patients on the basis of their personal and cultural preferences and may therefore have the best chance for long-term success.




FIGURE 26-3


Reduction in waist circumference in overweight or obese subjects.

(From Sacks FM, Bray GA, Carey VJ, et al. Comparison of weight-loss diets with different compositions of fat, protein, and carbohydrates. N Engl J Med 2009;360(9):859-873.)


Shai and colleagues conducted a randomized trial in 322 overweight or obese people that found that a Mediterranean diet or a low-carbohydrate, high-protein Atkins diet produced similar weight loss after 2 years and slightly more than a low-fat diet. The Atkins diet group had the most weight loss early in the trial but also had the most weight regain. Finally, Foster and colleagues compared the effects of an Atkins diet with a low-fat diet in a 2-year randomized trial and found no difference.


The Look AHEAD (Action for Health in Diabetes) was a multicenter randomized clinical trial to compare the effects of an intensive lifestyle intervention and diabetes support and education on incidence of major CVD events in overweight and obese individuals with type 2 diabetes mellitus. Averaged over 4 years, the intensive lifestyle intervention produced better weight loss and improvements in fitness, glycemic control, and CVD risk factors.


These long-term diet interventions support the accomplishment of weight loss sustained over an extended period (2 years and more) in overweight and obese individuals by several dietary and behavioral approaches. Dietary patterns influenced weight gain during 20 years in large cohorts of middle-aged and older U.S. women and men. Foods associated with weight gain were potato chips, potatoes, sugar-sweetened beverages, and red meats. Foods associated with weight loss were vegetables, whole grains, fruits, nuts, and yogurt.


Clinical Assessment of Obesity


Body mass index (BMI), expressed as weight in kilograms divided by height in meters squared (kg/m 2 ), is commonly used to classify overweight. BMI does not measure percentage of body fat. The BMI of an individual who weighs 180 pounds and is 67 inches tall is calculated as follows:


<SPAN role=presentation tabIndex=0 id=MathJax-Element-1-Frame class=MathJax style="POSITION: relative" data-mathml='180lb÷2.2kg/lb=81.8kg’>180lb÷2.2kg/lb=81.8kg180lb÷2.2kg/lb=81.8kg
180 lb ÷ 2.2 kg / lb = 81.8 kg

<SPAN role=presentation tabIndex=0 id=MathJax-Element-2-Frame class=MathJax style="POSITION: relative" data-mathml='67in×2.54=170.2cm=1.7m’>67in×2.54=170.2cm=1.7m67in×2.54=170.2cm=1.7m
67 in × 2.54 = 170.2 cm = 1.7 m

<SPAN role=presentation tabIndex=0 id=MathJax-Element-3-Frame class=MathJax style="POSITION: relative" data-mathml='BMI=81.8kg÷(1.7)2=28.3kg/m2′>BMI=81.8kg÷(1.7)2=28.3kg/m2BMI=81.8kg÷(1.7)2=28.3kg/m2
BMI = 81.8 kg ÷ ( 1.7 ) 2 = 28.3 kg / m 2


A BMI table is shown in Table 26-3 .



TABLE 26-3

Body Mass Index (BMI) Table


















































































































































































































































































































































































































































































































































































































































































































































































































































































BMI 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35
HEIGHT (in) WEIGHT (lb)
58 91 96 100 105 110 115 119 124 129 134 138 143 148 153 158 162 167
59 94 99 104 109 114 119 124 128 133 138 143 148 153 158 163 168 173
60 97 102 107 112 118 123 128 133 138 143 148 153 158 163 168 174 179
61 100 106 111 116 122 127 132 137 143 148 153 158 164 169 174 180 185
62 104 109 115 120 126 131 136 142 147 153 158 164 169 175 180 186 191
63 107 113 118 124 130 135 141 146 152 158 163 169 175 180 186 191 197
64 110 116 122 128 134 140 145 151 157 163 169 174 180 186 192 197 204
65 114 120 126 132 138 144 150 156 162 168 174 180 186 192 198 204 210
66 118 124 130 136 142 148 155 161 167 173 179 186 192 198 204 210 216
67 121 127 134 140 146 153 159 166 172 178 185 191 198 204 211 217 223
68 125 131 138 144 151 158 164 171 177 184 190 197 203 210 216 223 230
69 128 135 142 149 155 162 169 176 182 189 196 203 209 216 223 230 236
70 132 139 146 153 160 167 174 181 188 195 202 209 216 222 229 236 243
71 136 143 150 157 165 172 179 186 193 200 208 215 222 229 236 243 250
72 140 147 154 162 169 177 184 191 199 206 213 221 228 235 242 250 258
73 144 151 159 166 174 182 189 197 204 212 219 227 235 242 250 257 265
74 148 155 163 171 179 186 194 202 210 218 225 233 241 249 256 264 272
75 152 160 168 176 184 192 200 208 216 224 232 240 248 256 264 272 279
76 156 164 172 180 189 197 205 213 221 230 238 246 254 263 271 279 287
BMI 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54
HEIGHT (in) WEIGHT (lb)
58 172 177 181 186 191 196 201 205 210 215 220 224 229 234 239 244 248 253 258
59 178 183 188 193 198 203 208 212 217 222 227 232 237 242 247 252 257 262 267
60 184 189 194 199 204 209 215 220 225 230 235 240 245 250 255 261 266 271 276
61 190 195 201 206 211 217 222 227 232 238 243 248 254 259 264 269 275 280 285
62 196 202 207 213 218 224 229 235 240 246 251 256 262 267 273 278 284 289 295
63 203 208 214 220 225 231 237 242 248 254 259 265 270 278 282 287 293 299 304
64 209 215 221 227 232 238 244 250 256 262 267 273 279 285 291 296 302 308 314
65 216 222 228 234 240 246 252 258 264 270 276 282 288 294 300 306 312 318 324
66 223 229 235 241 247 253 260 266 272 278 284 291 297 303 309 315 322 328 334
67 230 236 242 249 255 261 268 274 280 287 293 299 306 312 319 325 331 338 344
68 236 243 249 256 262 269 276 282 289 295 302 308 315 322 328 335 341 348 354
69 243 250 257 263 270 277 284 291 297 304 311 318 324 338 338 345 351 358 365
70 250 257 264 271 278 285 292 299 306 313 320 327 334 341 348 355 362 369 376
71 257 265 272 279 286 293 301 308 315 322 329 338 343 351 358 365 372 379 386
72 265 272 279 287 294 302 309 316 324 331 338 346 353 361 368 375 383 390 397
73 272 280 288 295 203 310 318 325 333 340 348 355 363 371 378 386 393 401 408
74 280 287 295 303 311 319 326 334 342 350 358 365 373 381 389 396 404 412 420
75 287 295 303 311 319 327 335 343 351 359 367 375 383 391 399 407 415 423 431
76 295 304 312 320 328 336 344 353 361 369 377 385 394 402 410 418 426 435 443

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Mar 21, 2019 | Posted by in GENERAL | Comments Off on Cardiovascular Disease and Lifestyle Modification
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